Fig. 6

A model depicting selective removal of ΔmtDNA during development and gametogenesis of C. elegans. A Schematic representation—high ΔmtDNA levels (red) associate with reduced egg hatching and delayed development. B Schematic representation of mitochondria in the gonad, carrying intact +mtDNA (black) and ΔmtDNA (red). Mitochondria in fzo-1(wt) oocytes form an intracellular mitochondrial network suggested to enable mitochondrial functional complementation, hence allowing ΔmtDNA inheritance. In contrast, in fzo-1(mut) animals, the fusion machinery is compromised, mitochondria are fragmented, suggesting that ΔmtDNA molecules are ‘exposed’ and hence selectivity eliminated in the gonad of fzo-1(mut);+/ΔmtDNA. C Two possible non-mutually exclusive mechanisms can explain the selective removal of ΔmtDNA molecules in the gonad of fzo-1(mut);+/ΔmtDNA. Signals from mitochondria are suggested to trigger programmed cell death of germ cells when the transition from a globular to a tubular organization is disrupted, as in fzo-1(mut) (left). Sperm-derived signals are suggested to trigger lysosome acidification in mature oocytes, which can activate mitophagy (right). These processes can selectively impact the removal of mitochondria with high levels of ΔmtDNA, respectively, in fzo-1(mut) animals. The figure was created in part using BioRender.com